Sep. 5, 2014
By Jacob Sullum
Here is a warning you will never see on a pack of cigarettes: “The Surgeon General Has Determined That Cigarette Smoking May Enhance Your Enjoyment of Cocaine.” Even for people who consider enhanced enjoyment of cocaine a drawback rather than an advantage, that risk probably would pale beside cancer, heart disease, and emphysema. But if you wanted to scare people away from a nicotine delivery product that poses none of those hazards, you might resort to warning them that it could prime their brains for cocaine pleasure. And that is exactly what Columbia neuropsychiatrist Eric Kandel and his wife, Columbia epidemiologist Denise Kandel, do in an article published by the New England Journal of Medicine this week.
The article is mostly devoted to a description of experiments in which the Kandels dosed mice with nicotine and cocaine. They found that the former enhanced the effects of the latter, as measured by activity levels, conditioned place preference, and various brain responses. The Kandels view these results as evidence to support their theory that “gateway drugs” such as tobacco, alcohol, and marijuana physiologically prime people to enjoy other psychoactive substances. They also think their mouse research is a reason to be wary of electronic cigarettes:
Although e-cigarettes eliminate some of the morbidity associated with combustible tobacco, they and related products are pure nicotine-delivery devices. They have the same effects on the brain as those reported here for nicotine…and they pose the same risk of addiction to other drugs and experiences….Whether e-cigarettes will prove to be a gateway to the use of combustible cigarettes and illicit drugs is uncertain, but it is clearly a possibility.
Clearly a possibility! More than enough for a new drug panic. “E-Cigarettes Are Gateway to Substance Abuse and Addiction,” Time declared. “New study suggests e-cigarettes are a ‘gateway drug,'” said The Week. The New York Daily News warned that “e-cigarettes could be a gateway to hard drugs.” According to Forbes.com health writer Melanie Haiken, the Kandels’ research “shows” that “e-cigarettes may be a ‘gateway’ drug for teenagers.”
Keep in mind that the Kandels’ research pertains to nicotine in general, not e-cigarettes specifically. So whatever the risk that nicotine will lead to cocaine, it applies equally to conventional cigarettes (as well as FDA-approved nicotine replacement products) and therefore does not count as an argument against switching from smoking to vaping, which dramatically reduces health hazards by eliminating tobacco and combustion (as even the Kandels begrudgingly acknowledge).
But what about the children? The Kandels mention the possibility that teenagers who otherwise would never smoke tobacco might decide to do so after trying e-cigarettes, even though the research they are discussing has nothing to do with that issue. Here is how a recent review in the journal Addiction summarized the empirical basis for the fear that vaping will lead to smoking:
Although there have been claims that EC [electronic cigarettes] is acting as a “gateway” to smoking in young people, the evidence does not support this assertion. Regular use of EC by non-smokers is rare and no migration from EC to smoking has been documented (let alone whether this occurred in individuals not predisposed to smoking in the first place). The advent of EC has been accompanied by a decrease rather than increase in smoking uptake by children.
There is even less evidence that vaping is boosting cocaine consumption, which has been declining since e-cigarettes were introduced. Furthermore, notes Carl Phillips of the Consumer Advocates for Smoke-Free Alternatives Association (CASAA), “cocaine use peaked long after smoking rates had come down, exactly the opposite of what [the Kandels] predict.”
In leaping from mouse to man, the Kandels make reckless assumptions about psychology and the nature of addiction. It is not at all clear that the data they gathered from rodents in their laboratory are relevant to humans living in the real world. “This study tells us little about human biology and nothing at all about real-world human behavior,” says Phillips. “It does not even measure mouse behavior. The study provides no evidence there is a gateway effect, and there is no reason to believe there is one.” CASAA President Julie Woessner calls it “a classic case of someone with a political agenda tacking their opinions onto technical research and trying trick the press into reporting it that way.” Fortunately for the Kandels, the press is easy to trick.
The Hazards of E-Cigarettes ASHRAE Journal, June 2014
By Francis (Bud) J. Offermann, P.E.,CIH, Member Ashrae
Read
http://bookstore.ashrae.biz/journal/download.php?file=2014June_038-047_IAQ_Offerman_rev.pdf
12/18/2013
Here is a silly NYTimes reporter’s analysis of the risk of breathing small particle-tainted air. As Milloy always says–show us the bodies. No fair just counting deaths, got to do a medical investigation.
Ok so start with small particles that come from cigarettes, agricultural activity, industrial activity, internal combustion engines–lots of different sources, probably of different toxicity, No?
The EPA and its running dog researchers do observational studies that are worthless, since they show small associations in the context of uncontrolled and even unknown confounders and monitors that only measure particles by size.
Then they just do the Cargo Cult game of authoritative number crunching for “associations” and blow smoke about small associations.
They harvest daily death count variations and claim a signal for toxic causation. Sure it is.
They claim a small particle premature death effect at a lag time of 1 or 2 or 3 days. That’s why I have never seen such a death–it’s a number derived from counting deaths, not investigating them. Killing people in a couple of days? Really? Even if the small particles exposure was very toxic, I could keep somebody severely and lethally damaged alive for a long time on a ventilator–what’s the answer to that?
Milloy always points out the basic problem of unknown exposures for death counts. Outside, inside, as a clear problem with the studies that run on outside air monitors when people are indoors more than 80 percent of the time. Another confounder that can’t be eliminated.
Toxicologists always point out that small particle is size, and doesn’t determine toxicity assuming that all sources are toxic ignores basic toxicology. Weaponized anthrax dust is similar in particle size to talcum powder. Agricultural dust can’t possibly be the same toxicity as industrial source emissions? Get the point?
Note that the claims of deaths based on the junk science projections range into the millions for small particles with no attempt to really determine what’s premature, or what was the nature of the exposure or the toxicity of the small particle load inhaled.
Of course you might also note the loose use of “premature” deaths. The researchers don’t do life expectancy analysis for the deaths.
And so now we have something that completely overwhelms the pea sized brain of a journalist who doesn’t understand toxicology and epidemiology and how the EPA researchers lie. However he does know the claims of deaths and he knows air pollution bad, smoking bad.
All the premature deaths studies that are the basis of EPA claims made to the US Congress that they are trying to stop hundreds of thousands of deaths each year from small particles are flawed and misuse the concept of premature death. The studies are counting deaths and matching elevated death rates against air pollution monitor reports, without regard to exposure confounding or even life expectancy. The researchers are harvesting the variability of death rates against computer dredging for a corresponding blip in small particle reports.
Smoking Risk
Cigarette smoking results in a pack/year increase in lung cancer so lifetime smokers have a 10 % risk of lung cancer, and the Relative Risk (RR) for smokers is 900 % or an RR of 10. It is time sensitive though, so if you stop smoking your RR will return to close to non smokers, if you stop soon enough, like before 10 years. The amount smoked is important–dose does make the poison.
Second hand smoking even in the data tortured meta analyses of the EPA and the Surgeon General shows an RR of 1.2 and yet they claim one breath of SHS is deadly–sure thing when you’re on a roll you can claim anything, its called lying for justice in politics or lying for a cause in the nanny state. Can’t be too careful–a good scare will have the right effect on behavior even if exaggerated. Precautionary principle kicks in. Some studies show no risk at all for second hand smoke (shs), environmental tobacco smoke(ets) so then the question is does one study refute a stack of studies that use bad methodology?
Here is a fine discussion by the Milloy
http://junkscience.com/2012/12/03/whats-epa-smoking/
Human exposure experiments
The EPA authorized and funded human exposure experiments with small particles at 10 domestic medical research facilities, 9 of them medical schools. Imagine Human exposure experiments with substances claimed by the sponsor to be lethal and carcinogenic.
Milloy and I were involved in investigating the human experiments and the filing of a lawsuit to stop them, American Traditions Institute v EPA.
Our position was why would the EPA sponsor and fund human exposure experiments with small particles when the EPA administrator said in testimony before congress that small particles were lethal and caused hundreds of thousands of deaths in America every year. Jon Samet MD said that there is no safe level of small particles, and he is the Chair of the Clean Air Scientific Advisory Committee of the EPA.
Robert Devlin, PhD, lead researcher at the North Carolina Lab that was doing human exposure experiments specified in the lawsuit, explained why the EPA was doing human exposure experiments.
From para 1 of his Declaration under penalty of perjury
“I am a Senior Scientist (ST) for the Environmental Public Health Division (EPHD), National Health and Environmental Research Laboratory (NHEERL), Office of Research and Development (ORD), U.S. Environmental Protection Agency. As one of three STs in NHEERL I am expected to be a scientific leader in the area of air pollution research, to define important areas of research, assemble teams to carry out that research and ensure it is completed in a timely manner and published in peer-reviewed journals. I am currently on detail as Acting Associated Director for Health for NHEERL. Prior to my current position, I was Chief of the Clinical Research Branch (CRB) of the EPHD from 1994 – 2008. The CRB is responsible for doing nearly all controlled human exposure studies within NHEERL.”
Then from para 7 and 8 of the same declaration.
“Epidemiological observations are the primary tool in the discovery of risks to public health such as that presented by ambient PM2.5. However, epidemiological studies do not generally provide direct evidence of causation. They indicate the existence or lack of a statistical relationship between ambient levels of PM2.5 and adverse health outcomes. Large population studies cannot assess the biological mechanisms (called biological plausibility) that could explain how inhaling ambient air pollution particles can cause illness or death in susceptible individuals. This sometimes leaves open the question of whether the observed association in the epidemiological study is causal or whether PM2.5 is merely a marker for some other unknown substance.
8. Controlled human exposure studies conducted by EPA scientists and EPA funded scientists at multiple universities in the United States fill an information gap that cannot be filled by large population studies.”
Back to Second Hand Smoke.
The studies on non smoking spouses of smokers have never shown an adequate relative risk association for evidence of carcinogenicity. The EPA and the smoking ban forces use faulty studies to push a strategy to stop smokers and stigmatize smokers as a toxic nuisance.
The smoking ban forces just pound the table in the absence of good evidence of toxicity and carcinogenicity of Second Hand Smoke.
It is not surprising that the NYT can’t get it right. An army of junk scientists has been working for more than 2 decades to create a smoky (pardon the pun) environment for evaluating air pollution and second hand smoke toxicology.
Babies in womb exposed to ‘gender-bending’ chemicals
By EMILY COOK
9-10-06
Babies are being exposed to “gender-bending” chemical pesticides before they are even born, disturbing new evidence has showed.
Tests on blood taken from the placentas of pregnant women revealed up to fifteen different types of pesticide, the research found.
Worryingly, the chemicals were found in every single one of the 308 women tested.
The findings will fuel concern about the chemicals, known as hormone disruptors or EDCs – endocrine-disrupting chemicals.
High levels of exposure have been linked to reproductive abnormalities – so-called gender-bending – because they upset the hormonal development of the embryo.
The effects are already being seen in nature where some species of fish and animals with deformed sex organs have been found.
Scientists blame agricultural pesticides and other hazardous chemicals such as those found in flame retardants which have leaked into the environment.
Last year a similar report by WWF-UK and Greenpeace found that babies are being exposed to a whole array of chemicals at the most vulnerable point in their development.
Tests on the blood of 30 newborn babies found the presence of eight different groups of chemicals, ranging from cleaning products to chemicals used to make plastics and non-stick waterproof coatings.
A study led by scientists at the University of Rochester in New York also found that common chemicals found in thousands of household products such as soaps and make-up can harm the development of unborn baby boys.
The results reinforce calls for pregnant women to be especially careful about their diet and for the reduction of chemicals in food production.
The latest findings were made by the Department of Radiology and Physical Medicine at the University of Granada in Spain.
Analysis of the placentas revealed the “presence of seventeen endocrine disruptive organochlorine pesticides” – the so-called gender benders.
Some patients’ placentas contained 15 of the 17 pesticides tested for.
Maria Jose Lopez Espinosa, who headed the research, feared that the chemicals could cause health problems for children who suffered exposure in the womb.
She said: “The results are alarming: 100 per cent of these pregnant women had at least one pesticide in their placenta but the average rate amounts to eight different kinds of chemical substances.”
She warned, “We do not really know the consequences of exposure to pesticides in children but we can predict that they may have serious effects since this placenta exposure occurs at key moments on the embryo’s development.”
The modern, chemical-laden environment can be especially harmful to pregnant women. During the gestation period, contaminants which accumulate in fatty tissues, access the unborn child via the blood supply and the placenta.
The Spanish research was carried out at San Cecilio University Hospital among 308 women who had given birth between 2000 and 2002. Tests were performed on 668 samples.
The study also found a higher presence of pesticides in older mothers and those who had a higher Body Mass Index.
Miss Espinosa believed that a healthy lifestyle with plenty of exercise, good food and no smoking would help combat the effect of “inadvertent exposure” to the chemicals.
She added, “It is possible to control pesticide ingestion by means of a proper diet, which should be healthy and balanced, through consumption of food whose chemical content is low.
“Moreover, daily exercise and the avoidance of tobacco, which could also be a source of inadvertent exposure, are very important habits which help to control the presence of pesticides in our bodies”.
SECOND-RATE SCIENCE
By ELIZABETH M. WHELAN
ENVIRONMENTAL activists this week brought the credibility of the noble science of epidemiology (the study of the cause of human disease) to another low.
The Air Resources Board of the California EPA declared that exposure to second-hand smoke upped a woman’s risk of breast cancer. Nevermind that the “study” was preliminary and was neither peer reviewed nor published.
The national media picked up its scary conclusions in a generally uncritical manner, most scientists remained silent on the travesty and the California regulatory exorcists who are committed to removing all “toxins” from the air, pondered even more legislation to “protect” women from breast cancer by eliminating exposure to second-hand smoke.
But there is no persuasive evidence that smoking, no less second-hand exposures, cause breast cancer. In fact, there is some evidence that women who smoke may have a reduced risk of breast cancer given that smoking reduces the body’s natural estrogen levels. Commonsense suggests that if a woman smoking a pack a day is not at increased risk of breast cancer, then a nonsmoking woman transiently exposed to second-hand smoke would not be either.
Indeed, why do anti-smoking advocates need to exaggerate their claims when there is already overwhelming scientific evidence of the dangers of smoking? Because the anti-smoking movement is driven by a zeal to regulate cigarette smoking out of existence and the ends justify the means.
They seem unaware that their baseless health claims threaten the acceptance and credibility of legitimate public health initiatives as facts and hype get tangled.
Let’s not give the tobacco industry fertile grounds for claiming all smoking and health claims are based on junk science.
Dr. Elizabeth M. Whelan is president, American Council on Science and Health.
http://www.nypost.com/
